May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Cigarette smoke–related oxidants and the development of sub–RPE deposits in an experimental mouse model
Author Affiliations & Notes
  • I.J. Suner
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
    Ophthalmology, Miami Veterans Affairs Medical Center, Miami, FL
  • D.G. Espinosa–Heidmann
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • N.Z. Gregori
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • E.P. Hernandez
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • S.W. Cousins
    Ophthalmology, Bascom Palmer Eye Institute, Miami, FL
  • Footnotes
    Commercial Relationships  I.J. Suner, None; D.G. Espinosa–Heidmann, None; N.Z. Gregori, None; E.P. Hernandez, None; S.W. Cousins, None.
  • Footnotes
    Support  Veterans Affairs Merit Review Grant
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1810. doi:
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      I.J. Suner, D.G. Espinosa–Heidmann, N.Z. Gregori, E.P. Hernandez, S.W. Cousins; Cigarette smoke–related oxidants and the development of sub–RPE deposits in an experimental mouse model . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1810.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Oxidative injury to the retinal pigment epithelium (RPE) has been proposed to be an important injury stimulus relevant to the accumulation of subretinal deposits in age–related macular degeneration (AMD). Although oxidants derived from blue light exposure or endogenous metabolic processes are more frequently implicated, we hypothesize that other environmental oxidants may also contribute to deposit formation. Cigarette smoking is the strongest environmental risk factor for all forms of AMD. Cigarette smoke–related tar contains high concentrations of a potent oxidant, hydroquinone. We investigated the effects of cigarette smoke (CS) and oral hydroquinone (HQ) in the development of sub RPE deposits in an experimental mouse model. Methods: 16–month old C57BL/6 mice were fed high–fat diet (HFD), then subdivided into Group I: HFD only, Group II: HFD + blue light, Group III: HFD + CS, and HFD + HQ. Mice were euthanized at 4.5 months and eyes processed for transmission electron microscopy. Results: As previously demonstrated by our lab and others, most mice fed high fat diet without other oxidant exposure demonstrated normal morphology or in a few cases small nodular basal laminar deposits. Mice exposed to a high fat diet + blue light demonstrated mild to moderately severe basal laminar deposits, moderate thickening of Bruch’s membrane and variable changes in the choriocapillaris endothelium. Eyes exposed to whole cigarette smoke demonstrated variable degree of basal laminar deposit. However, those specimens demonstrated the presence of monocytes within choriocapillaris lumens or infiltrating into choriocapillaris pillars. In addition, several animals demonstrated monocytes in the sub RPE space. Bruch’s membrane was diffusely thickened with homogenous material. The choriocapillaris endothelium was variably hypertrophic. Finally, mice exposed to oral hydroquinone demonstrated moderately thick basal laminar deposits and variable degree of deposits within Bruch’s membraneConclusion: Exposure to cigarette smoke, or the smoke–related oxidant hydroquinone, results in the formation of sub–RPE deposits, thickening of Bruch’s membrane, and accumulation of deposits within Bruch’s membrane. In addition, smoke–exposed animals demonstrated low–grade inflammatory infiltration. Smoke related oxidants may be another oxidative injury stimulus to the choriocapillaris and RPE, and may explain the association between cigarette smoking and macular degeneration.

Keywords: age–related macular degeneration • choroid • drug toxicity/drug effects 

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